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Dual protective mechanisms of matrix metalloproteinases 2 and 9 in immune defense against Streptococcus pneumoniae

Jeong-Soo Hong1, Kendra J Greenlee, Ramanan Pitchumani

  • 1Section of Pulmonary and Critical Care, Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|April 22, 2011
PubMed

Insights

Matrix metalloproteinases (MMPs) are crucial for lung defense against Streptococcus pneumoniae. MMP2 and MMP9 are vital for bacterial clearance and host survival during pneumonia, highlighting their nonredundant roles in innate immunity.

Area of Science:

  • Immunology
  • Microbiology
  • Biochemistry

Background:

  • Effective innate immune responses are critical for host survival against bacterial pathogens.
  • Understanding local innate immune mediators in lung defense against pathogens is essential for elucidating host defense mechanisms.

Purpose of the Study:

  • To investigate the roles of matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, in the innate immune response to Streptococcus pneumoniae lung infection.
  • To determine the impact of MMP2 and MMP9 deficiency on host survival, bacterial burden, immune cell recruitment, and inflammatory mediator levels during pneumococcal pneumonia.

Main Methods:

  • Utilized a murine model of acute Streptococcus pneumoniae lung infection.
  • Compared survival rates, lung bacterial burdens, and polymorphonuclear leukocyte (PMN) recruitment between wild-type and Mmp2/9(-/-) mice.
  • Quantified levels of cytokines and chemokines (IL-17A, IP-10, RANTES) in lung tissue.
  • Assessed the impact of MMP2 and MMP9 on bacterial phagocytosis and reactive oxygen species (ROS) generation by neutrophils.

Main Results:

  • Mmp2/9(-/-) mice exhibited a survival disadvantage compared to wild-type controls following S. pneumoniae infection.
  • Mmp2/9(-/-) mice had increased lung polymorphonuclear leukocyte infiltration but higher bacterial burdens.
  • Elevated levels of IL-17A, IP-10, and RANTES were observed in the lungs of Mmp2/9(-/-) mice.
  • MMP2 partially inactivated IL-17A, while MMP9 was essential for efficient bacterial phagocytosis and ROS production in neutrophils.

Conclusions:

  • MMP2 and MMP9 play critical, nonredundant, and protective roles in the early innate immune response against Streptococcus pneumoniae lung infection.
  • MMP9 is particularly important for neutrophil-mediated bacterial clearance mechanisms.
  • Dysregulation of MMP activity impacts host defense outcomes during pneumococcal pneumonia.

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